Toxic Pneumonitis
Exposure: Industrial Spills, Fires, and Confined Space Accidents
"Short-term exposures to high concentrations of noxious gases, fumes,
or mists generally are a result of industrial or transportation accidents or
fires." [LaDou, p. 312)
Mechanism: Direct Cellular Injury
Acute toxic pneumonitis is caused by acute irritant injury and also by
several other mechanisms: heavy metal pneumonitis, hydrocarbon aspiration,
paraquat lung injury, and inhalation fever. [Murray, p. 1824]
"The site of deposition of an inhaled gas is determined primarily by
its water solubility, but also by the duration of exposure and minute
ventilation of the victim. [Sullivan, p. 224]
"Respirable particles with diameters in the 0.3-0.5 um range can
bypass the upper airways and deposit in the more distal airways and alveoli.
The clinical consequences of these injuries include diffuse bronchiolar
inflammation and obstruction as well as alveolar filling (pulmonary edema). [Rosenstock,
p. 333]
Toxic Inhalation Hazard (TIH)
"Term used to describe gases and volatile liquids that are toxic when
inhaled." [ERG 2012]
The mechanism of toxicity after
inhalation of a material includes:
Simple asphyxia (nitogen and
methane)
Tissue asphyxia (carbon monoxide,
cyanide, and hydrogen sulfide)
Nonrespiratory effects
(hydrocarbon solvents and lead)
Stimulation of physiological
responses (formaldehyde, sulfur dioxide)
Direct cellular injury (ammonia,
chlorine, nitrogen dioxide, and phosgene) [Sullivan, Table 17-1]
"In acute pulmonary injury from inhaled irritants, exposure is
typically brief and intense; initial symptom onset occurs within minutes to
24-48 hours after exposure. . . . Any irritant (high or low solubility) can
cause pulmonary edema after sufficient exposure. . . . Heavy metal pneumonitis
is clinically similar to irritant inhalation injury. As with low solubility
gases, upper-airway mucous membrane irritation is minimal; thus, the exposure
may have poor warning properties. Offending agents include cadmium, mercury,
and in limited industrial settings, nickel carbonyl." [Olson, p.
530]
"Some agrichemicals may cause
toxic pneumonitis after non-inhalatory exposure. The best known of these
agents is the herbicide paraquat which gains access to the lung via the
circulation after gastrointestinal or (rarely) dermal absorption, and exerts a
selective toxicity for the pulmonary epithelium." [Hendrick, p. 208]
Cause: Many Corrosive Gases and Vapors Plus Metal Fumes and Low-Solubility
Gases (Phosgene, Ozone, and NO2)
In addition to cadmium and mercury, other metals (antimony, manganese, and
beryllium) have been reported as causes of acute pneumonitis, but in the last
50 years there have been few reports to document such disorders. [Murray, p.
1827]
The major irritant airborne toxicants are ammonia (making plastics and
fertilizer), bromine (making specialty chemicals), chlorine (plastics industry
and water treatment), chlorine dioxide (making paper and food preparation),
diborane (microelectronics), ethylene oxide (gas sterilizing), formaldehyde
(embalmers, hospital workers, and making home furnishings and building
materials), hydrogen chloride (chemical industry and firefighters), hydrogen
fluoride (plastics and microelectronics), methyl isocyanate (pesticide
manufacturing), nitrogen dioxide (welding and agriculture), ozone (arc
welding, textile, and printing), phosgene (making isocyanates and pesticides
and welding), sulfur dioxide (petroleum refining, smelting, making paper, and
refrigeration). [LaDou, Table 30-4]
Effects: Non-Cardiogenic Pulmonary Edema
The potential effects of inhaled irritants include irritation (eyes,
nose, and throat), laryngeal edema (upper airway), tracheobronchitis (lower
airway), and pneumonitis/pulmonary edema/adult respiratory distress syndrome
(lung parenchyma). [LaDou, Table 20-2]
In this chapter, toxic
pneumonitis refers to acute or subacute disorders of chemically induced injury
in the lung parenchyma. . . . many agents that can cause toxic tracheo-bronchitis
may also cause toxic pneumonitis, and some overlap is inevitable among disease
descriptions." [Hendrick, p. 201]
Disease Definition in Haz-Map
In this database,
agents linked to toxic pneumonitis are divided into two categories: primary
and secondary. The primary chemicals can cause acute pneumonitis in animal
experiments and are listed as toxic inhalation hazards (TIH) or releasers of
TIH gases when spilled in water according to the 2012
Emergency Response Guidebook. These chemicals are linked to the
occupational disease "Pneumonitis, toxic." The secondary chemicals
are not linked to the occupational disease, but they are tagged with "Toxic
Pneumonitis" as an adverse effect. Because of their importance in
work-related exposures, cadmium fume, welding fumes, ozone, and elemental
mercury vapor are also linked to the occupational disease even though they are
not designated TIH. Also, all chemicals in the category "Corrosive
Gases" are linked to the occupational disease.
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